Angiogenesis, the development and growth of new blood vessels, is important for organ development, wound healing and various pathological conditions such as tumor growth or proliferative retinopathies. Neovascularization depends on adhesive contacts of the endothelial cells with the extracellular matrix, on endothelial cell migration and sprouting, as well as on the function of growth factors. There is emerging evidence that inflammatory cells regulate endothelial cell functions related to angiogenesis. 1) CCN1 is an immediate early gene that acts as a ligand of alphavbeta3-integrin and thereby mediates endothelial cell adhesion and migration. We could demonstrate that VEGF upregulates CCN1 in osetoblasts and this CCN1 acts to attract endothelial cells and to assist in neovascularization in the context of repair angiogenesis. 2) The participation of the complement system in hypoxia-driven retina angiogenesis and in tumor angiogenesis is currently under investigation by using complement components and inhibitors and genetically modified mice. 3) Hypoxia induces replication arrest in cells that may result in DNA damage. Nevertheless, in hypoxia-induced angiogenesis, such as during retinopathy of prematurity, endothelial cells need to actively proliferate due to the presence of hypoxia-inducible factors. To understand this paradox we study the DNA damage response to hypoxia in endothelial cells. Hypoxia induced a rapid DNA-damage response in endothelial cells. In vitro and in vivo studies revealed that this DNA repair response due to hypoxia helps endothelial cells overcome the hypoxia-induced replication arrest, thus promoting hypoxia-driven angiogenesis.